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Android apps become increasingly memory-demanding as software vendors add more and more new features to their apps. In the mean time, Android users often launch multiple apps and conveniently switch back and forth among the apps. Although running multiple apps imposes a high pressure on memory management, virtual-memory swap, an essential feature to improve the degree of multitasking, is disabled in fear of premature retirement of flash-based storage devices. Instead, Android employs a termination-based, process-level memory reclaiming method. We observed that process killing is, unfortunately, not effective in memory reclaiming and is highly negative to user experience. In this study, we advocate re-thinking using swap in Android for improved user experience with managed write stress on flash storage. Based on a series of empirical analyses of swap activities, we propose an enhanced page replacement policy and a page-compressing frontswap module. The proposed page replacement policy jointly considers page activeness and compressibility to boost the compression ratio of swap writes. A sampled-based method for page compressibility prediction is introduced so that decisions on page replacement can be made without compressing every page. We also design a frontswap module that strategically organizes compressed pages in the swap space for reducing the overhead of swap I/O operations. Experimental results showed that compared with process killing, our method improved the app launching time and energy consumption by 58% and 19%, respectively; compared with the original swap, our approach reduced the swap write stress by 65%.

Pigment disorder dermatoses are common diseases with complex mechanisms. There are various methods for the clinical treatment of pigmentation diseases, but these have a poor curative effect and many adverse reactions. Currently, looking for safe and effective whitening agents is a popular research topic. Stromal vascular fractions (SVFs) are a compound cell component of adipose-derived stem cells (ADSCs) that can promote tissue regeneration, healing, and vascularization. The purpose of this experiment was to investigate the inhibitory effect of SVFs on pigmentation in guinea pigs.After guinea pig subcutaneous fat was digested and centrifuged, SVFs were isolated and quantified. SVF was injected into the pigmentation area of the prepared guinea pig pigmentation model. The amount of inducible nitric oxide synthase (iNOS) was determined using immunohistochemical analysis, histopathological staining, and the Fontana-Masson (F-M) method for measuring melanin formation.The skin of the guinea pigs obtained stable and homogenous coloration following three treatments with narrow-band ultraviolet B (NB-UVB). Hematoxylin-eosin (HE) staining revealed that compared to the control group, the cuticle, granular layer, and spinous layer were thicker and the number of epidermal melanocytes and melanin granules increased. While the quantity of pigment granules in the treated group dramatically decreased, it did not significantly change in the blank control group. F-M staining revealed that melanin granules greatly expanded following ultraviolet irradiation and were continuously distributed in basal cells and spinous layers. The entire epidermis was evenly covered in melanin granules. The level of melanin dramatically decreased following therapy. According to immunohistochemical labeling, epidermal cells' cytoplasm and membranes are where iNOS is primarily found. In the epidermis of the irradiated group, iNOS expression was much higher than in the control group, and following treatment, it decreased in the experimental group.SVFs have a reliable treatment effect on ultraviolet B (UVB)-induced pigmentation in guinea pig skin. SVFs can significantly inhibit pigmentation, effectively shorten the fading time of pigmentation, and play a role in skin whitening, providing a new breakthrough for the treatment of pigmentation diseases.

During the long coevolution of human cytomegalovirus (HCMV) and humans, the host has formed a defense system of multiple layers to eradicate the invader, and the virus has developed various strategies to evade host surveillance programs. The intrinsic immunity primarily orchestrated by promyelocytic leukemia (PML) nuclear bodies (PML-NBs) represents the first line of defense against HCMV infection. Here, we demonstrate that microrchidia family CW-type zinc finger 3 (MORC3), a PML-NBs component, is a restriction factor targeting HCMV infection. We show that depletion of MORC3 through knockdown by RNA interference or knockout by CRISPR-Cas9 augmented immediate-early protein 1 (IE1) gene expression and subsequent viral replication, and overexpressing MORC3 inhibited HCMV replication by suppressing IE1 gene expression. To relief the restriction, HCMV induces transient reduction of MORC3 protein level via the ubiquitin-proteasome pathway during the immediate-early to early stage. However, MORC3 transcription is upregulated, and the protein level recovers in the late stages. Further analyses with temporal-controlled MORC3 expression and the major immediate-early promoter (MIEP)-based reporters show that MORC3 suppresses MIEP activity and consequent IE1 expression with the assistance of PML. Taken together, our data reveal that HCMV enforces temporary loss of MORC3 to evade its repression against the initiation of immediate-early gene expression.

Refereed/Peer-reviewed Oxidative stress plays a crucial role in the pathophysiology of diastolic dysfunction associated with diabetic cardiomyopathy. Novel oral edaravone (OED) alleviates oxidative stress by scavenging free radicals and may be suitable for the treatment of chronic diseases such as diabetic cardiomyopathy. Oral administration of OED to type 2 diabetic rats (induced by high-sugar/high-fat diet and intraperitoneal injection of streptozotocin) for 4 w decreased malondialdehyde and increased superoxide dismutase. Moreover, it significantly improved ratios of early to late diastolic peak velocity, myocardium hypertrophy accompanied by decreased cross-sectional areas of cardiomyocytes, the proportion of apoptotic cells, collagen volume fractions, and deposition of collagen I/III. In H9c2 cells, OED reduced reactive oxygen species, cell surface area, and numbers of terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling-positive cells induced by glucolipotoxicity. OED remarkably upregulated expression of the nuclear factor E2-related factor (Nrf2) signaling pathway both in vivo and in vitro. In addition, OED promoted Nrf2 nuclear translocation and upregulated nicotinamide adenine dinucleotide phosphate quinone oxidoreductase and heme oxygenase. Silencing of Nrf2 abolished the protective effect of OED in H9c2 cells. Our findings demonstrate that OED has the therapeutic potential to ameliorate diastolic dysfunction associated with diabetic cardiomyopathy. Its effect was mainly achieved by attenuating hyperglycemia and hyperlipidemia-induced cardiomyocyte hypertrophy, apoptosis, and fibrosis by activating the Nrf2 signaling pathway.

Background: To investigate the MicroRNA-146a targeting regulation of IL-6/STAT3 signaling pathway activity and influence the proliferation and apoptosis behavior-related mechanisms of OA chondrocytes. Material and Methods: 10 C57 mice were isolated and cultured with membrane protease and type II collagenase. The experiment was divided into blank group, MicroRNA-146a overexpression group and low expression group. The chondrocytes were transfected with plasmid vector. After 48 hours of culture, the proliferation rate of chondrocytes was detected by MTT method. The levels of type ii collagen, MMP-9, IL-1, IL-6, and TNF-α in culture medium were detected by ELISA. Luciferase reported experimental analysis of MircoRNA-146a targeting regulation of IL-6 genes. Results: Compared with the blank group, the proliferation rate of chondrocytes in the overexpression group was significantly decreased, the apoptosis rate was increased, the levels of IL-6 and p-STAT3 protein, type II collagen, MMP-9, IL-1, IL-6 and TNF-α were increased, while the low expression group was correlated (P < 0.05). Luciferase reporter experiments confirmed that MicroRNA-146a had a better binding effect with the IL-6 gene. Conclusion: MicroRNA-146a overexpression may mediate activation of IL-6/STAT3 signaling pathway and participate in decreased proliferation activity and increased apoptosis activity in OA chondrocytes. IL-6 gene may have targeted regulatory sites for MicroRNA-146a.

Network function virtualization (NFV) enables network operators to save costs and flexibility by replacing dedicated hardware with software network functions running on commodity servers. There is a high need for network acceleration to achieve performance comparable to hardware, which is vital for the implementation of NFV. The necessity of NFV acceleration stems from the lengthy packet delivery path following virtualization and the unavailability of generic operating system designs to serve network-specific scenarios. Therefore, the software approach alters the operating system’s processing architecture through Kernel Bypass or offload packet processing to hardware. A typical classification scheme divides it into two main categories based on technology with software and hardware. Only these two categories can be utilized to rapidly and easily establish a classification system. However, it is difficult to suggest the specifics and peculiarities of any acceleration approach during real-world operation. For a more comprehensive classification of NFV acceleration, we refer to the ETSI NFV architectural framework in this research. As the framework clearly illustrates, the technical infrastructure layer of NFV and the corresponding management roles provides a comprehensive and intuitive view of the differences between these acceleration technologies, solutions, and initiatives. Additionally, we conducted an analysis to identify opportunities for improvement in existing solutions and propose new research programs. We expect that NFV will increasingly rely on cloud services in the future. Since cloud services do not offer a choice of hardware, our acceleration method will be primarily software-based.

Herbicide safeners selectively protect crops from herbicide damage without reducing the herbicidal efficiency on target weed species. The title compounds were designed by the intermediate derivatization approach and fragment splicing to exploit novel potential safeners. A total of 31 novel diazabicyclo derivatives were synthesized by the microwave-assistant method using isoxazole-4-carbonyl chloride and diazabicyclo derivatives. All synthetic compounds were confirmed by infrared, 1H and 13C nuclear magnetic resonance, and high-resolution mass spectrometry. The bioassay results demonstrated that most of the title compounds could reduce the nicosulfuron phytotoxicity on maize. The glutathione S-transferase (GST) activity in vivo was assayed, and compound 4(S15) revealed an inspiring safener activity comparable to commercialized safeners isoxadifen-ethyl and BAS-145138. The molecular docking model exhibited that the competition at the active sites of target enzymes between compound 4(S15) and nicosulfuron was investigated with respect to herbicide detoxification. The current work not only provided a powerful supplement to the intermediate derivatization approach and fragment splicing in design pesticide bioactive molecules but also assisted safener development and optimization.

Background Diastolic dysfunction is the most common change of diabetic cardiomyopathy (DCM), but there is no effective clinical treatment at present. Oxidative stress plays a crucial role in the pathophysiological process of diabetic diastolic dysfunction including hypertrophy, apoptosis and fibrosis. The novel Oral-edaravone (OED) alleviates oxidative stress by scavenging free radical and may be suitable for the treatment of chronic diseases such as DCM. Methods DCM was induced by high sugar and high fat diet with intraperitoneal injection of streptozotocin (STZ) in rats. OED (3mg/kg/day) was administration for 4 weeks. Cardiac structure and function were measured using transthoracic echocardiography. H9C2 cardiomyocytes with Nrf2 transfection or not were incubated in glucolipotoxicity and treated with OED for 48 hours to further explore the mechanism. Results In type 2 diabetic rats,oral administration of OED for 4 weeks decreased malondialdehyde (MDA) and increased superoxide dismutase (SOD). OED significantly improved E/A ratio and myocardium hypertrophy accompanied by decreased cross-sectional area of cardiomyocytes, proportion of apoptotic cells, collagen volume fractions and depositions of collagen I/III. In H9C2 cells, OED reduced reactive oxygen species (ROS), cell surface area and TUNEL-positive cells induced by glucolipotoxicity. OED remarkably up-regulated the expression of the Nrf2 signaling pathway both in vivo and in vitro, further promoted Nrf2 nuclear translocation and up-regulated nicotinamide adenine dinucleotide phosphate quinone oxidoreductase (NQO1) and heme oxygenase (HO-1). Moreover, Nrf2 gene silencing abolished the protective effect of OED in H9c2 cells. Conclusion Our findings demonstrated that OED treatment has the therapeutic potential to ameliorate diastolic dysfunction of DCM. The effect is mainly achieved by attenuating hyperglycemia and hyperlipidemia-induced cardiomyocytes hypertrophy, apoptosis and fibrosis via activating the Nrf2 signaling pathway.